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CHD), persistently elevated pulmonary artery pressure can cause right heart failure and even death [6,7]. Thus, it is imperative to explore more accurate biomarkers and new therapeutic targets for PAH
CHD.CircRNAs constitute a unique category of non-coding RNA molecules, which is a well-established fact. Compared with linear RNA, circRNA molecules show a closed-loop structure, have higher stability, and are therefore less susceptible to degradation [8]. Recent studies have elucidated that circRNAs harbor binding sites for microRNAs (miRNAs), functioning as a sponge to sequester these miRNAs and thereby relieve their inhibitory effects on target genes. It is due to this mechanism that circRNAs have been clarified to interact with miRNAs to regulate the occurrence and development of various diseases [[9], [10], [11]]. Interestingly, relevant literature reported that there were many differentially expressed circRNAs in neonatal PAH
CHD patients [12].MiRNAs are endogenous small RNAs that serve as an essential factor in gene expression, either at the translational or the transcriptional level [13]. At present, more and more studies have shown that the miRNAs family has a crucial relationship with the development of PAH [14,15]. Hu F et al. proved that miRNA-30d-5p adjusted the apoptosis of HPASMCs by targeting the Notch-3 signaling pathway [16]. It was confirmed that miR-153 targets ROCK1 and NFATc3 to abolish abnormal proliferation and metastasis of HPASMCs caused by hypoxia [17]. However, there are few studies on the function and mechanism of circRNAs in PAH
CHD. Our research aims to clarify the relationship between circRNAs and miRNAs and circRNAs involved in PAH
CHD pathogenesis.
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